Alzaid Fawaz, Fagherazzi Guy, Riveline Jean-Pierre, Bahman Fatemah, Al-Rashed Fatema, Al-Mulla Fahd, Ahmad Rasheed
Dasman Diabetes Institute, Kuwait City, Kuwait.
INSERM UMR-S1151, CNRS UMR-S8253, Université Paris Cité, Institut Necker Enfants Malades, Paris, France.
Diabetologia. 2025 Jun 4. doi: 10.1007/s00125-025-06437-z.
Adipose tissue, once regarded merely as an energy reservoir, has emerged as a critical regulator of both metabolic and immune processes. This paradigm shift has profound implications for understanding and managing type 1 diabetes, a condition typically associated with lean individuals. The growing global prevalence of obesity has introduced an underexplored dimension to type 1 diabetes pathophysiology, a phenomenon that has significant consequences for disease development, progression and management. The coexistence of obesity and type 1 diabetes presents unique challenges, including exacerbation of insulin resistance and an elevated risk of complications such as CVD. Obesity-induced chronic low-grade inflammation, or 'meta-inflammation', creates a proinflammatory environment within adipose tissue. This disrupts systemic immune regulation, promotes insulin resistance and may even potentiate autoimmunity directed to pancreatic beta cells. Addressing these interactions will allow us to reframe research priorities and the management of type 1 diabetes in individuals who also live with obesity. In this review, we explore how adipose tissue maladaptation in obesity influences the pathophysiology of type 1 diabetes. We discuss existing literature and gaps in knowledge, and emphasise the importance of addressing these gaps. We also highlight the potential of emerging technologies and precision medicine to tackle the dual challenge of obesity and type 1 diabetes. Advances such as continuous glucose monitoring and automated insulin delivery systems and insights from genomics and metabolomics are revolutionising diabetes care. These tools can enhance glucose management and provide opportunities to mitigate weight-related complications and personalise treatment strategies.
脂肪组织，曾经仅仅被视为一个能量储存库，如今已成为代谢和免疫过程的关键调节因子。这一范式转变对于理解和管理1型糖尿病具有深远意义，1型糖尿病通常与体型偏瘦的个体相关。全球肥胖患病率的不断上升为1型糖尿病的病理生理学引入了一个尚未充分探索的层面，这一现象对疾病的发生、发展和管理具有重大影响。肥胖与1型糖尿病的共存带来了独特的挑战，包括胰岛素抵抗的加剧以及诸如心血管疾病等并发症风险的升高。肥胖诱导的慢性低度炎症，即“代谢性炎症”，在脂肪组织内营造了一种促炎环境。这扰乱了全身免疫调节，促进胰岛素抵抗，甚至可能增强针对胰腺β细胞的自身免疫。解决这些相互作用将使我们能够重新调整研究重点以及对同时患有肥胖症的1型糖尿病患者的管理方式。在这篇综述中，我们探讨肥胖状态下脂肪组织适应不良如何影响1型糖尿病的病理生理学。我们讨论现有文献以及知识空白，并强调填补这些空白的重要性。我们还强调新兴技术和精准医学在应对肥胖和1型糖尿病双重挑战方面的潜力。连续血糖监测和自动胰岛素输送系统等进展以及基因组学和代谢组学的见解正在彻底改变糖尿病护理。这些工具可以加强血糖管理，并为减轻与体重相关的并发症以及使治疗策略个性化提供机会。
